中国科学院行为科学重点实验室知识库

Risk-taking is a concerning yet prevalent issue during adolescence and can be life-threatening. Examining its etiological sources and evolving pathways helps inform strategies to mitigate adolescents' risk-taking behavior. Studies have found that unfavorable environmental factors, such as adverse childhood experiences (ACEs), are associated with momentary levels of risk-taking in adolescents, but little is known about whether ACEs shape the developmental trajectory of risk-taking. Even less research has investigated the underlying mechanisms. Drawing on the self-regulation theory, this study examined the associations between ACEs and the developmental trajectory of adolescent risk-taking. Moreover, it also explored self-control as a mediator and genetic variations as a moderator from a "gene x environment" approach. Participants were 564 Chinese adolescents (48.40% males, Mage = 14.20 years, SD = 1.52). Adolescents reported their ACEs and self-control at T1 and risk-taking three times, with a six-month interval between each time point. Adolescents' saliva was collected at T1 for genetic extraction, and polygenetic index was created based on the gene-by-environment interaction between SNPs and ACEs for self-control via the leave-one-out machine learning approach. Findings of latent growth modeling revealed that adolescents' risk-taking decreased over time. ACEs were directly and indirectly through self-control associated with high initial levels of, and a rapid decrease in, risk-taking, especially for those with a higher polygenetic index compared to those with a lower polygenetic index. Theoretically, these results suggest a tripartite model of adolescent risk-taking, such that risk-taking is the combined function of adverse experiences in early years, low self-control, and carriage of sensitive genes. Practically, intervention strategies should reduce childhood adversities, build up self-control, and consider the potential impacts of genetic plasticity.